Melanotan I

Background:Homogenous pigmentation can be induced by α-melanocyte-stimulating hormone (MSH) homologues. Cosmetically inacceptable pigmentation is mostly located on the face.Objectives:Although afamelatonide is a prescription drug for the orphan disease erthropoetic protoporphyria, structurally related α-MSH derivatives are available via the internet. Preventive and therapeutical options are necessary for postinflammatory hyperpigmentation, melasma, and lentigines.Methods:Case reports address activation of dysplastic naevi by melanotan I. Wood's lamp is of some use in analyzing the level of hyperpigmentation. However, no guidelines have been established; thus, a summary of current studies is presented.Results:Melanotan I leads to the activation of dysplastic nevi. The gold standard for hyperpigmentation is triple therapy with hydrochinon, tretinoin, and steroids, which can cause irritation and lead to ochronosis in some individuals. Tyrosinase inhibitors, substances that increase the cell turnover, and plant derivatives are less efficient but more tolerable.Conclusions:Melanotan I and bleaching creams, which may possibly contain mercury, are dangerous. Hyperpigmentation is best treated using a combination therapy that inhibits melanocyte activity and melanin synthesis, removes melanin, destroys melanin granules, and includes UV protection. Especially in Fitzpatrick skin types IV-VI, cryotherapy and laser are not the first line treatment options due to renewed posttreatment hyperpigmentation.

The effects of melanotan-II, a non-specific agonist of melanocortin receptors, on erection and its possible sites of action were investigated in anesthetized rats. Delivered i.v. (0.1, 0.3 and 1 mg/kg) or within the paraventricular nucleus of the hypothalamus (0.1 and 1 microg), melanotan-II exerted a dose-dependent inducer activity on erection by eliciting erectile events and shortening latency of the first erectile event to occur. Erectile events were of higher amplitude in rats treated with melanotan-II i.t. (0.2 microg) delivered at the L6-S1 level than in animals treated with the vehicle i.t. delivered. Erectile responses elicited by cavernous nerve stimulation were increased after i.v. melanotan-II (1 mg/kg), thereby exerting facilitator effect on erection. In contrast, melanotan-II injected within the corpus cavernosum (1 microg) did not display any facilitator activity. To investigate the neural pathways involved in the facilitator effect of melanotan-II, we performed acute spinalization (T8 level) and differential selective nerve transections. Neither spinalization nor bilateral transection of pelvic nerves or dorsal penile nerves impaired facilitator activity of i.v. melanotan-II (1 mg/kg). Conversely, the facilitator effect of melanotan-II was abolished after acute removal of the lumbar paravertebral sympathetic chain. These results lead to the conclusion that central and peripheral melanocortin pathways are recruited by melanotan-II, depending on its route of delivery, to exert both inducer and facilitator activities on erection.

Renal infarction is an uncommon condition resulting from an acute disruption of renal blood flow and it is potentially life-threatening disease. The cause and outcome of renal infarction is not well established and is frequently misdiagnosed or diagnosed late. Melanotan II is a non-selective melanocortin-receptor agonist and its effect on humans is an increasing of skin pigmentation, producing of spontaneous penile erection and sexual stimulation. Melanotan II inducing rhabdomyolysis and renal failure have been described previously. We present a review of Melanotan II and the possible effects of this drug on the kidneys by including a case of a renal infarction most likely attributed to Melanotan II. In the mechanism of renal injury with Melanotan II, thrombotic pharmacological influence and possible direct toxic effect on renal parenchyma must be considered.